Cellular Senescence Program

The Cellular Senescence Program researches the basic biology of aging.

Learning more about what drives the body to age may ultimately lead to ways to prevent or reverse conditions associated with aging and to improvements in health span — the healthy, productive time in life.

One of the most significant biological processes behind aging is cellular senescence. To maintain health, most cells in the body continually divide to replace old and damaged tissue. But eventually cells age and stop dividing.

The cells that have stopped the normal biological process of dividing are called senescent cells. Senescent cells secrete inflammatory proteins that destroy or impair the function of healthy cells around them. This destruction contributes to organ dysfunction and the development of age-related disorders throughout the body, including cancer, cardiovascular disease, stroke, dementia, mobility disorders, arthritis, osteoporosis and metabolic diseases.

Focus areas

The Cellular Senescence Program has several research focus areas:

  • Eliminating dysfunctional senescent cells
  • Suppressing the release of toxic factors that are secreted by senescent cells
  • Understanding and interfering with the pathways that drive aging

Research in these focus areas will help the program gain better understanding of the basic biology of aging and identify the molecules and pathways that drive cellular senescence and aging.

Findings from this research may ultimately lead to new ways to modulate senescent cells, thus delaying or reversing diseases and disabilities associated with aging.

Research findings

Research findings from the Cellular Senescence Program include:

  • Discovering drugs that selectively eliminate senescent cells (senolytic drugs).
  • Discovering a causal link between senescent cells and osteoarthritis in mice.
  • Showing that senescent cells negatively impact health and shorten life span by as much as 35% in normal mice.
  • Discovering methods for reducing age-related stem cell dysfunction and metabolic disease, including diabetes, in naturally aged mice.
  • Finding that inhibiting key enzyme pathways reduces inflammation in human cells in culture dishes and decreases inflammation and frailty in aged mice.
  • Engineering laboratory mice with senescent cells and then evaluating the impact on the health span of the mice when a drug was used to systematically eliminate the senescent cells. The researchers found that elimination of senescent cells delayed the onset of age-related disorders in the mice. The New York Times called this process "a delicate feat of genetic engineering."

Program leadership

Director: James L. Kirkland, M.D., Ph.D.